Mitochondrial dysfunction is a possible cause of accelerated senescence of mesothelial cells exposed to high glucose

Biochemical and Biophysical Research Communications

Volumn 366, Issue 3, 2008, Pages 793-799

  Ksiazek, Krzysztof ^a,b   Passos, João F ^b   Olijslagers, Sharon ^b   von Zglinicki, Thomas ^b  

^a POZNAN UNIVERSITY OF MEDICAL SCIENCES   (Poland)

^b NEWCASTLE UNIVERSITY   (United Kingdom)

Author keywords

Accelerated senescence; DNA damage; High glucose; Mesothelial cells; Mitochondria; Oxidative stress

Indexed keywords

DOUBLE STRANDED DNA; GLUCOSE; LIPOFUSCIN; PEROXIDE; REACTIVE OXYGEN METABOLITE; SCAVENGER; SUPEROXIDE;

ARTICLE; BIOMECHANICS; CELL AGING; CELL FUNCTION; CONTROLLED STUDY; DISORDERS OF MITOCHONDRIAL FUNCTIONS; DNA STRAND BREAKAGE; GENOME; HUMAN; HUMAN CELL; IN VITRO STUDY; INNER CELL MASS; MEMBRANE POTENTIAL; MESOTHELIUM CELL; MITOCHONDRIAL MEMBRANE; MITOCHONDRION; PERITONEUM CELL; PRIORITY JOURNAL; SENESCENCE; TELOMERE;

CELL AGING; CELLS, CULTURED; DNA DAMAGE; DOSE-RESPONSE RELATIONSHIP, DRUG; EPITHELIUM; GLUCOSE; HUMANS; MITOCHONDRIA; OXIDATIVE STRESS;

EID: 37549050960     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2007.12.021     Document Type: Article

References (31)

1. Chen Q.M. Replicative senescence and oxidant-induced premature senescence. Beyond the control of cell cycle checkpoints. Ann. NY Acad. Sci. 908 (2000) 111-125
2. von Zglinicki T., Saretzki G., Docke W., and Lotze C. Mild hyperoxia shortens telomeres and inhibits proliferation of fibroblasts a model for senescence?. Exp. Cell Res. 220 (1995) 186-193
3. Chen Q.M., Prowse K.R., Tu V.C., Purdom S., and Linskens M.H. Uncoupling the senescent phenotype from telomere shortening in hydrogen peroxide-treated fibroblasts. Exp. Cell Res. 265 (2001) 294-303
4. Rolo A.P., and Palmeira C.M. Diabetes and mitochondrial function: role of hyperglycemia and oxidative stress. Toxicol. Appl. Pharmacol. 212 (2006) 167-178
5. Cerami A. Hypothesis glucose as a mediator of aging. J. Am. Geriatr. Soc. 33 (1985) 626-634
6. Loots M.A., Lamme E.N., Mekkes J.R., Bos J.D., and Middelkoop E. Cultured fibroblasts from chronic diabetic wounds on the lower extremity (non-insulin-dependent diabetes mellitus) show disturbed proliferation. Arch. Dermatol. Res. 291 (1999) 93-99
7. Blazer S., Khankin E., Segev Y., Ofir R., Yalon-Hacohen M., Kra-Oz Z., Gottfried Y., Larisch S., and Skorecki K.L. High glucose-induced replicative senescence: point of no return and effect of telomerase. Biochem. Biophys. Res. Commun. 296 (2002) 93-101
8. Mutsaers S.E., and Wilkosz S. Structure and function of mesothelial cells. Cancer Treat. Res. 134 (2007) 1-19
9. Sitter T., and Sauter M. Impact of glucose in peritoneal dialysis: saint or sinner?. Perit. Dial. Int. 25 (2005) 415-425
10. Mortier S., De Vriese A.S., and Lameire N. Recent concepts in the molecular biology of the peritoneal membrane-implications for more biocompatible dialysis solutions. Blood Purif. 21 (2003) 14-23
11. Gotloib L., Shostak A., Wajsbrot V., and Kushnier R. High glucose induces a hypertrophic, senescent mesothelial cell phenotype after long in vivo exposure. Nephron 82 (1999) 164-173
12. Ksiazek K., Korybalska K., Jorres A., and Witowski J. Accelerated senescence of human peritoneal mesothelial cells exposed to high glucose: the role of TGF-beta1. Lab. Invest. 87 (2007) 345-356
13. Ksiazek K., Breborowicz A., Jorres A., and Witowski J. Oxidative stress contributes to accelerated development of the senescent phenotype in human peritoneal mesothelial cells exposed to high glucose. Free Radic. Biol. Med. 42 (2007) 636-641
14. Yung S., Li F.K., and Chan T.M. Peritoneal mesothelial cell culture and biology. Perit. Dial. Int. 26 (2006) 162-173
15. Ksiazek K., Piwocka K., Brzezinska A., Sikora E., Zabel M., Breborowicz A., Jorres A., and Witowski J. Early loss of proliferative potential of human peritoneal mesothelial cells in culture: the role of p16INK4a-mediated premature senescence. J. Appl. Physiol. 100 (2006) 988-995
16. von Zglinicki T., Pilger R., and Sitte N. Accumulation of single-strand breaks is the major cause of telomere shortening in human fibroblasts. Free Radic. Biol. Med. 28 (2000) 64-74
17. McGinn S., Poronnik P., King M., Gallery E.D., and Pollock C.A. High glucose and endothelial cell growth: novel effects independent of autocrine TGF-beta 1 and hyperosmolarity. Am. J. Physiol. Cell Physiol. 284 (2003) C1374-C1386
18. Sibbitt Jr. W.L., Mills R.G., Bigler C.F., Eaton R.P., Griffey R.H., and Vander Jagt D.L. Glucose inhibition of human fibroblast proliferation and response to growth factors is prevented by inhibitors of aldose reductase. Mech. Ageing Dev. 47 (1989) 265-279
19. Terman A., and Brunk U.T. Oxidative stress, accumulation of biological 'garbage', and aging, Antioxid. Redox Signal. 8 (2006) 197-204
20. Sitte N., Merker K., Grune T., and von Z.T. Lipofuscin accumulation in proliferating fibroblasts in vitro: an indicator of oxidative stress. Exp. Gerontol. 36 (2001) 475-486
21. Terman A., and Brunk U.T. Lipofuscin. Int. J. Biochem. Cell Biol. 36 (2004) 1400-1404
22. von Zglinicki T., Saretzki G., Ladhoff J., d'Adda di Fagagna F., and Jackson S.P. Human cell senescence as a DNA damage response. Mech. Ageing Dev. 126 (2005) 111-117
23. Lorenzi M., Montisano D.F., Toledo S., and Barrieux A. High glucose induces DNA damage in cultured human endothelial cells. J. Clin. Invest. 77 (1986) 322-325
24. Song F., Jia W., Yao Y., Hu Y., Lei L., Lin J., Sun X., and Liu L. Oxidative stress, antioxidant status and DNA damage in patients with impaired glucose regulation and newly diagnosed Type 2 diabetes. Clin. Sci. (Lond.) 112 (2007) 599-606
25. Ksiazek K., Passos J.F., Olijslagers S., Saretzki G., Martin-Ruiz C., and von Zglinicki T. Premature senescence of mesothelial cells is associated with non-telomeric DNA damage. Biochem. Biophys. Res. Commun. 362 (2007) 707-711
26. d'Adda di Fagagna F., Reaper P.M., Clay-Farrace L., Fiegler H., Carr P., von Zglinicki T., Saretzki G., Carter N.P., and Jackson S.P. A DNA damage checkpoint response in telomere-initiated senescence. Nature 426 (2003) 194-198
27. Shostak A., Wajsbrot V., and Gotloib L. High glucose accelerates the life cycle of the in vivo exposed mesothelium. Kidney Int. 58 (2000) 2044-2052
28. Passos J.F., von Zglinicki T., and Saretzki G. Mitochondrial dysfunction and cell senescence: cause or consequence?. Rejuvenation Res. 9 (2006) 64-68
29. Lee H.B., Yu M.R., Song J.S., and Ha H. Reactive oxygen species amplify protein kinase C signaling in high glucose-induced fibronectin expression by human peritoneal mesothelial cells. Kidney Int. 65 (2004) 1170-1179
30. Yano M., Hasegawa G., Ishii M., Yamasaki M., Fukui M., Nakamura N., and Yoshikawa T. Short-term exposure of high glucose concentration induces generation of reactive oxygen species in endothelial cells: implication for the oxidative stress associated with postprandial hyperglycemia. Redox Rep. 9 (2004) 111-116
31. Passos J.F., Saretzki G., Ahmed S., Nelson G., Richter T., Peters H., Wappler I., Birket M.J., Harold G., Schaeuble K., Birch-Machin M.A., Kirkwood T.B., and von Zglinicki T. Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence. PLoS Biol. 5 (2007) e110